The CCN1 Knockout HEK293T Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population in which CCN1 has been disrupted. Derived from HEK293T, this pooled loss-of-function model preserves genetic diversity while abrogating CCN1 expression, rendering it ideal for population-level functional assays examining adhesion, migration, proliferation, and signaling.
The host HEK293T line is an immortalized human embryonic kidney derivative expressing SV40 large T antigen, enabling episomal plasmid propagation and conferring high transfection efficiency. Widely used for protein expression and virus production, its well-characterized signaling landscape and adherent growth provide a consistent platform for gene knockout studies. The embryonic kidney origin offers a neutral context to investigate CCN1 without specialized tissue constraints.
CCN1 (CYR61) is a secreted matricellular protein that bridges integrins (??v??3, ??v??5, ??6??1) and heparan sulfate proteoglycans, thereby activating focal adhesion kinase (FAK) and Src. This stimulates ERK/MAPK and PI3K/AKT cascades, culminating in the modulation of YAP/TAZ and NF-??B transcription factors. CCN1 expression is induced by TGF-??, EGF, VEGF, FGF2, and hypoxia, and the protein interacts with decorin, fibronectin, and LRP1. Downstream, it regulates genes such as cyclin D1, Bcl-2 family members, and matrix metalloproteinases (MMPs), thereby coordinating cell cycle progression, survival, matrix remodeling, and inflammatory responses. Through these interactions, CCN1 integrates signals from integrin, Wnt, TGF-??, and Hippo pathways to control tissue homeostasis, angiogenesis, and wound healing.
In HEK293T cells, CCN1 knockout provides a clean background to dissect its signaling functions without lineage-specific noise. The polyclonal nature averages out clonal variations, ensuring reproducible population-level phenotypes. Adherent growth and transfection competence facilitate direct measurement of CCN1-dependent adhesion dynamics, migration, and anchorage-dependent proliferation. Moreover, the knockout simplifies interpretation of NF-??B, YAP/TAZ, ERK, and AKT activation analyses, enabling precise delineation of CCN1??s role in these pathways.
Applications include western blotting for CCN1 and phospho-proteins, transwell migration/invasion, cell adhesion assays, MTS/EdU proliferation, annexin V/PI apoptosis, integrin activation, luciferase reporters for NF-??B or YAP/TAZ, RNA-seq, and phospho-flow cytometry for ERK/AKT. These tools empower investigations into cancer metastasis, fibrosis, cardiovascular disease, inflammation, and wound healing, as well as high-throughput drug screening targeting CCN1-associated pathways. For further details, contact Ascent Research.
